Far infrared¬†radiation¬†(FIR) is currently investigated as a potential therapeutic strategy in various diseases though the mechanism is unknown. Presently, we tested if FIR mediates beneficial effects in a¬†cell¬†model¬†of the neurodegenerative disease¬†spinocerebellar¬†ataxia¬†type 3 (SCA3). SCA3 is caused by a mutation leading to an abnormal polyglutamine expansion (PolyQ) in ataxin-3¬†protein. The consequent aggregation of mutant ataxin-3 results in disruption of vital¬†cell¬†functions. In this study, neuroblastoma cells (SK-N-SH) was transduced to express either non-pathogenic ataxin-3-26Q or pathogenic ataxin-3-78Q proteins. The cells expressing ataxin-3-78Q demonstrated decreased¬†viability, and increased sensitivity to metabolic stress in the presence rotenone, an inhibitor of¬†mitochondrial¬†respiration. FIR exposure was found to protect against these effects. Moreover, FIR improved¬†mitochondrial¬†respiratory¬†function, which was significantly compromised in ataxin-3-78Q and ataxin-3-26Q expressing cells. This was accompanied by decreased levels of¬†mitochondrial¬†fragmentation in FIR treated cells, as observed by fluorescence microscopy and¬†protein¬†expression analysis. Finally, the expression profile LC3-II, Beclin-1 and p62 suggested that FIR prevent the autophagy inhibiting effects observed in ataxin-3-78Q expressing cells.